Doxorubicin-hydrochloride-Hydroxydaunorubicin-hydrochloride-DataSheet-生命科學(xué)試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEDoxorubicinhydrochlorideCat.No.:HY-15142CASNo.:25316-40-9Synonyms:Hydroxydaunorubicinhydrochloride;HydroxydaunorubicinHydrochloride分?式:C??H??ClNO??分?量:579.98作?靶點:Topoisomerase;ADCCytotoxin;AMPK;Autophagy;Apoptosis;HIV;HBV;Mitophagy;Antibiotic;Bacterial作?通路:CellCycle/DNADamage;Antibody-drugConjugate/ADCRelated;Epigenetics;PI3K/Akt/mTOR;Autophagy;Apoptosis;Anti-infection儲存?式:4°C,sealedstorage,awayfrommoistureandlight*Insolvent:-80°C,6months;-20°C,1month(sealed

storage,awayfrommoistureandlight)溶解性數(shù)據(jù)體外實驗DMSO:35.71mg/mL(61.57mM;ultrasonicandwarmingandheatto60°C)H2O:20mg/mL(34.48mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制備儲備液1mM1.7242mL8.6210mL17.2420mL5mM0.3448mL1.7242mL3.4484mL10mM0.1724mL0.8621mL1.7242mL請根據(jù)產(chǎn)品在不同溶劑中的溶解度選擇合適的溶劑配制儲備液；?旦配成溶液，請分裝保存，避免反復(fù)凍融造成的產(chǎn)品失效。儲備液的保存?式和期限：-80°C,6months;-20°C,1month(sealedstorage,awayfrommoistureandlight)。-80°C儲存時，請在6個?內(nèi)使?，-20°C儲存時，請在1個?內(nèi)使?。體內(nèi)實驗請根據(jù)您的實驗動物和給藥?式選擇適當(dāng)?shù)娜芙?案。以下溶解?案都請先按照InVitro?式配制澄的儲備液，再依次添加助溶劑：(為保證實驗結(jié)果的可靠性，澄的儲備液可以根據(jù)儲存條件，適當(dāng)保存；體內(nèi)實驗的?作液，建議您現(xiàn)?現(xiàn)配，當(dāng)天使?；以下溶劑前顯?的百分?指該溶劑在您配制終溶液中的體積占?；如在配制過程中出現(xiàn)沉淀1/4MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE、析出現(xiàn)象，可以通過加熱和/或超聲的?式助溶)1.請依序添加每種溶劑：10%DMSO>>40%PEG300>>5%Tween-80>>45%salineSolubility:≥2.08mg/mL(3.59mM);Clearsolution2.請依序添加每種溶劑：10%DMSO>>90%(20%SBE-β-CDinsaline)Solubility:≥2.08mg/mL(3.59mM);Clearsolution3.請依序添加每種溶劑：5%DMSO>>40%PEG300>>5%Tween-80>>50%salineSolubility:≥2.75mg/mL(4.74mM);ClearsolutionBIOLOGICALACTIVITY?物活性Doxorubicin(Hydroxydaunorubicin)hydrochloride?種具有細胞毒性的蒽環(huán)類抗?素，?種抗癌化療試劑。Doxorubicinhydrochloride?種有效的?類DNAtopoisomeraseI和topoisomeraseII抑制劑，IC50分別為0.8μM和2.67μM。Doxorubicinhydrochloride可降低AMPK及其下游靶蛋??酰輔酶A羧化酶的磷酸化。還可誘導(dǎo)凋亡(apoptosis)和?噬[1][2][3]。IC50&TargetTopoisomeraseITopoisomeraseIIDaunorubicins/DoxorubicinsHIV-10.8μM(IC50)2.67μM(IC50)體外研究Doxorubicinhydrochloride(1-8μM;24and48hours)decreasestheviabilityofMCF-10F,MCF-7andMDA-MB-231cellsinatime-anddose-dependentmanner[4].Doxorubicinhydrochloride(1μM;3and24hours)resultsinHct-116humancoloncarcinomacellsreductioninG0/G1phaseandaccumulationinG2phase[5].Doxorubicinhydrochloride(1μMforMCF-10FandMDA-MB-231cells,4μMforMCF-7cells;48hours)inducesapoptosisbyupregulatingBax,caspase-8andcaspase-3anddownregulationofBcl-2proteinexpression[4].CellViabilityAssay[4]CellLine:BreastcancercelllinesMCF-10F,MCF-7andMDA-MB-231Concentration:0,1,2,4and8μMIncubationTime:24and48hoursResult:IC50was1μMforbothMCF-10FandMDA-MB-231celllines.IC50was4μMforMCF-7cellline.CellCycleAnalysis[5]CellLine:Hct-116humancoloncarcinomacellsConcentration:1μMIncubationTime:3hoursand24hoursResult:Both,bolus(3h)andcontinuous(24h)incubationledtoasignificantreductionofcellsin2/4MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEG0/G1andaccumulationinG2phase.WesternBlotAnalysis[4]CellLine:BreastcancercelllinesMCF-10F,MCF-7andMDA-MB-231Concentration:1μMforMCF-10FandMDA-MB-231cells,4μMforMCF-7cellsIncubationTime:48hoursResult:BaxproteinexpressionwasupregulatedinMCF-10FandMDA-MB-231celllinesbutMCF-7cellsdidnotshowanysignificantincrease.Caspase-8geneexpressionwasupregulatedinMCF-10F,butitwasdownregulatedinMCF-7andMDA-MB-231cells.體內(nèi)研究TreatmentwithDoxorubicin(2mg/kg)orZoledronicacid(100μg/kg)alonedoesnotstatisticallysignificantlydecreasefinaltumorvolumecomparedwithsaline.MicetreatedwithDoxorubicinplusZoledronicacidhavestatisticallysignificantlysmallerfinaltumorvolumesthanthosetreatedwithDoxorubicinalone[6].AnimalModel:FemaleMF1nu/numicebearingMDA-G8breasttumorxenograft(6-week-old)[6]Dosage:Doxorubicin(2mg/kg);Zoledronicacid(100μg/kg)Administration:Intravenousinjection;onceaweek;6weeksResult:Moderateinhibitionofsubcutaneoustumorgrowthinmicethatweretreatedwith2mg/kgDoxorubicinaloneorwith100μg/kgZoledronicacidalonecomparedtothesalinecontrol.MicetreatedwithZoledronicacidandDoxorubicintogetherhadstatisticallysignificantsmallermeantumorvolumesonday42thanthosetreatedwithDoxorubicinalone.戶使?本產(chǎn)品發(fā)表的科研?獻?NatMed.2016May;22(5):547-56.?CellRes.2018Dec;28(12):1171-1185.?MilMedRes.2021Dec9;8(1):63.?CellMetab.2022Feb7;34(3):424-440.e7.?NatCellBiol.2020Sep;22(9):1056-1063.Seemorecustomervalidationsonwww.MedChemEREFERENCES3/4MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE[1].JohnL.Nitiss,etal.TargetingDNAtopoisomeraseIIincancerchemotherapy.NatRevCancer.2009May;9(5):338-50.[2].Hee-KyungRhee,etal.Synthesis,cytotoxicity,andDNAtopoisomeraseIIinhibitoryactivityofbenzofuroquinolinediones.BioorgMedChem.2007Feb15;15(4):1651-8.[3].PDFoglesong,etal.DoxorubicininhibitshumanDNAtopoisomeraseI.CancerChemotherPharmacol.1992;30(2):123-5.[4].NesstorPilco-Ferreto,etal.Influenceofdoxorubicinonapoptosisandoxidativestressinbreastcancercelllines.IntJOncol.2016Aug;49(2):753-62.[5].RegineLüpertz,etal.Dose-andtime-dependenteffectsofdoxorubicinoncytotoxicity,cellcycleandapoptoticcelldeathinhumancoloncancercells.Toxicology.2010May27;271(3):115-21.[6].PenelopeDOttewell,etal.Antitumoreffectsofdoxorubicinfollowedbyzoledronicacidinam